Hypoxia is not synonymous with an abnormal PaO₂ or SaO₂ on blood gas analysis and encompasses the inevitable oxygen debt and accumulation of lactic acid from anaerobic metabolism. The aims of resuscitation are to prevent further accumulation of oxygen debt and institute rapid repayment [4]. Of prime importance is the realization that despite normalizing DO₂, an oxygen debt must still be repaid as indicated by a persistently elevated lactate or base deficit.

Despite an acceptable level of arterial oxygen saturation, endotracheal intubation and mechanical ventilation should be employed liberally in patients with a lactic acidosis. The lungs are the main buffering mechanism by which humans compensate for an acute metabolic acidosis, renal compensation being slower and later, and removing the work of breathing may help substantially. The drug for induction and intubation must be carefully selected in order to avoid further cardiovascular instability, and ketamine and etomidate are the agents of choice despite the reported association of adrenal insufficiency with the latter [5]. This is a late and only potential risk, whereas the effects of hypotension are definite and acute.

Recently the concept of protective lung ventilation (PLV) has been advocated for the critically ill and injured [6], but this is not universally applicable in major trauma, especially during the acute phase. An adequate minute volume is required to buffer a metabolic acidosis; to avoid rises in intracranial pressure following TBI, hypercarbia must be prevented and tidal volumes may need to be higher than those proposed for PLV; and in patients with blunt thoracic trauma and a pulmonary contusion, a substantial proportion of damaged lung may be recruited by initially using higher tidal volumes between 8 and 10 ml/kg. Once recruited the tidal volume may be reduced as necessary, and lung volume maintained with positive end expiratory pressure (PEEP).

Major hemorrhage results in intravascular volume depletion and a significant drop in cardiac output and DO₂. Short periods of hypotension although causing cellular apoptosis result in complete recovery of ATP production, whereas protracted shock episodes cause cell necrosis and irreversible organ damage [7]. The conventional approach has been to restore intravascular volume with clear fluids, either crystalloid or colloid, and augment DO₂ later with blood transfusion. Although restoring intravascular volume and perfusion, clear fluids do not carry oxygen, and a proactive rather than reactive philosophy has recently been adopted with the early use of blood and blood products and limitation of clear resuscitation fluids. To this end a massive transfusion protocol must be established [8] whereby the necessary products are released urgently and as required with the aim of achieving a set ratio of packed red blood cells (PRBCs) to plasma and platelets. This has the desired effect of rapidly optimizing DO₂ and counteracting the effect of the acute coagulopathy of trauma. Experience from military conflicts suggested initially that PRBCs, plasma, and platelets should be administered in a 1:1:1 ratio [9], but evidence from the civilian environment indicates that a less aggressive plasma volume is superior with a PRBC to plasma ratio of 2:1 being preferred, thereby minimizing complications without affecting survival [10]. There is no role for supranormal DO₂, and the use of permissive hypotension is only applicable in the setting of uncontrolled hemorrhage where theater is immediately available. Sustained hypoperfusion results in irreversible organ ischemia and a physiological point of no return.